1. Field of the Invention
The present invention relates to compositions and formulations for the treatment of skin disorders or damage in various animals, including humans, and specifically the treatment of hypertrophic and keloid scar tissue, acute phototoxicity, hyperpigmented lesions, skin discoloration, keratosis, and skin hardening. More particularly, the present invention relates to particular formulations of such compositions and method of using the same for the treatment of the above skin disorders and similar problems.
2. Description of the Prior Art
It is known that the process of oxygen based metabolism through the conversion of food to energy forms the foundation of life. While oxidation/reduction (or "redox") reactions are essential to life processes, they also are known to contribute to the process of aging. Oxidation produces potentially toxic and destructive molecules known as free radicals, which are electrochemically unstable species of elements or molecules.
Free radicals have an unbalanced number of electrons when compared with stable counterparts, thus providing them with an electrical charge. As a result, free radicals tend to seek electrical balance by sharing electrons with surrounding stable molecules. This can create chain reactions of free radical production which can lead to serious cellular imbalance.
Even though free radicals are present in all biological systems and they perform necessary functions therein, they are also believed to be responsible for many of the problems with the body at a cellular level. If free radical production proceeds out of control, it can precipitate relentless destruction and degeneration of the body as a whole, including causing inflammation, cellular injury, and protein and cell destruction.
It is also known that a distinct relationship exists between aging and lipid peroxidation caused by the interaction of free radicals on fats and oils at a cellular level. These peroxides tend to join with other lipids and create more peroxides and free radicals. This can lead to serious damage to organelles in the cell, to the cell membrane, and to the ability of DNA and RNA in the cell to replicate. Peroxidation and free radicals are believed to be a primary cause of cell mutation and cancer. By protecting the body and tissues from oxy-stress (i.e. free radical and peroxide damage), it is believed that the rate of aging and susceptibility to disease can be dramatically reduced.
When free radicals react with molecules of protein in cell or tissue, long chain proteins become cross-linked (i.e. molecularly bound together and tangled). Cross-linking is also known to be accelerated by environmental factors, such as exposure to pollutants, heavy metals, and ultra-violet light and other forms of radiation.
Cross-linking of the protein collagen is a phenomenon fundamental to age degeneration. At an internal level, cross-linking of collagen is believed to cause arteriosclerosis and cancer; at a more superficial level, cross-linking can lead to skin wrinkling and sagging. Cross-linking of various proteins, such as collagen, elastin, and reticulin, also can lead to diminished ability of the cell to absorb and metabolize nutrients and to dispose of waste.
While a body is young, it produces special enzymes which are necessary for proper metabolism and which are effective at breaking down and preventing excessive cell cross-linking. One such group of enzymes are ubiquinones which contribute to a variety of cell functions, including the manufacture of adenosine triphosphate (ATP), as well as assisting in oxygen transfer, and acting as a antioxidant to protect cells from free radicals. Ubiquinones include vitamin K.sub.1, which serves as a antihemorrhagic agent, and the Q coenzymes, such as Co-Q.sub.4 through Q.sub.15. Coenzyme Q.sub.10 is produced in the liver and, as is discussed below, has been linked to a variety of beneficial results when taken internally.
As the body ages, accumulation of free radicals accelerates at the same time that the production of protective enzymes diminish. It is believed that the combined effect of these two factors contribute greatly to the process of aging. By way of example, Coenzyme Q.sub.10 has been identified as an important enzyme necessary in metabolism, a powerful antioxidant, and an immunostimulating agent. It is known that the body loses its ability to synthesize this molecule as it ages, leaving diet as the only source for it.
One study has shown that laboratory animals which were administered coenzyme Q.sub.10 internally had a 56% increase in longevity as compared with a control group. The coenzyme group also had more youthful appearance until the end of their lives.
Not surprisingly, considerable interest has been generated in studying the ubiquinones, and particularly coenzyme Q. U.S. Pat. No. 3,658,648, issued Apr. 25, 1972 to Nakao et al., discloses a process for the production of coenzyme Q. U.S. Pat. No. 4,156,718, issued May 29, 1979 to Bliznakov, discloses that internally administering coenzyme Q.sub.4 to Q.sub.13 to animals can be effective in controlling and reversing immunological senescence.
One of the major problems with coenzyme Q is that it is found in extremely low quantities in nature and has been relatively difficult to extract or chemically synthesize. Accordingly, it is expensive and of limited availability. As a result, a program of treatment employing coenzyme Q is necessarily constrained due to the expense of the coenzyme. For many common minor aging problems, such as loss of suppleness and elasticity of the skin (i.e. resulting in dryness, wrinkling and similar cosmetic problems), oral doses of coenzyme Q are not economically practical. Additionally, the quantity of oral doses of coenzyme are also constrained in that there is no way to target the coenzyme for a particular injury site; thus, total intake must be limited to avoid possible toxicity in the body as a whole.
Despite the successes with the internal administration-of coenzyme Q in controlling and reversing the process of aging in animals, prior to the present invention applicant was unaware of any instance where coenzyme Q was suggested to be used topically to address skin injury, aging or other damage. In fact, upon information and belief, even in treating periodontal diseases, treatment with coenzyme Q has been administered in oral doses transported through the blood system. Furthermore, there is a lack of teaching or suggestion in the literature concerning a method or formulation for providing optimal ubiquinone uptake by the skin.
Subsequent to the present invention, applicant has become aware of one instance where skin penetration of coenzyme Q.sub.10 was investigated in rats. Giovannini, L. et al., "Skin Penetration of CoQ.sub.10 in the Rat," 10 Int. J. Tissue React. 103-05 (1988). This study indicated that the coenzyme is absorbed by the skin of the rat at a rate proportional to its concentration when suspended in olive oil. However, the authors apparently did not investigate whether pharmacological treatment was possible or practical. Moreover, the authors provide no suggestion of particular formulations which may provide successful topical therapeutic treatment.
Although other substances have been employed to treat skin damage problems, none have proven fully satisfactory. Various vitamins, such as vitamin E, have been applied to skin alone and in conjunction with other preparations, but these have met with limited therapeutic success. Similarly, various preparations employing squalane and squalene have been applied to the skin, but these have also proven less than completely therapeutically acceptable.
Accordingly, it is a primary object of the present invention to provide a formulation and method for effectively treating skin damage in humans and other animals, including damage due to injury and aging.
It is a further object of the present invention to provide such a formulation and method which permits topical application of active chemical constituents directly to an injury site, allowing maximum doses with minimum risk of toxicity to other cells.
It is another object of the present invention to provide such a formulation and method which permits topical application to an injury site in order to avoid non-site waste of expensive chemical constituents, thus limiting the cost of treatment and making such treatment more widely available.
It is yet another object of the present invention to provide a formulation and method for the topical application of coenzyme Q to injury sites on skin.
It is an additional object of the present invention to provide a formulation and method for the topical application of coenzyme Q to injury sites on skin which maximizes the uptake and effectiveness of the coenzyme.
A still further object of the present invention is to provide a formulation and method for the topical application for the treatment of hypertrophic and keloid scar tissue, acute phototoxicity, hyperpigmented lesions, skin discoloration, keratosis, and skin hardening.
These and other objects of the present invention will become evident through review of the following specification.